MED SURGE II: RESP SYSTEM

Normal osmolality = 275-295mosm/kg

Average water intake 2500cc
Thirst main regulator of fluid intake
Kidneys: main regulator of fluid output ( Renin
system, and ADH).
 CRYSTALLOIDS= fluids with the same electrolyte
concentration as plasma. ( isotonic solutions:
lactated ringers and Normal saline).
 COLLOIDS= fluids used to expand plasma volume
and maintain blood pressure. * they remain in the
intravascular space. ( albumin, dextran)
 ELECTROLYTE LEVELS: major electrolyte in the ICF
= K 3.5 – 5.0 mEq/L ; ECF= Na 135-145
 MED SURGE II: RESP SYSTEM
 ABG’S ( compansated ( ph is normal and the other two are
not), uncompansated (when either bicab, or CO2 are
abnormal), partially compansated
 ph = 7.35- 7.45 ( <7.35 = acidic >7.45 = alkaline)
 paCO2: 35mmHG- 45mmHg (normal range)
< 35mmHg= base
> 45mmHg= acidic

 HCO3 < 22 = acidic

(22-26 range) >26 = metabolic
 RESP ACIDOSIS PATHO: pneumonia, pneumothorax, chronic
obstructive lung disease
 RESP ALKALOSIS PATHO: anxiety, hyperthyroidism, PE, pain
 MET ACIDOSIS: diarrhea, starvation, shock, kidney failure
 MET ALKALOSIS: severe vomitting, gastric suction, excess
blood
 MED SURGE II: RESP SYSTEM
PLEURAL EFFUSION:
- What is it? : accumulation of fluid in the pleural
space. Linked to other diseases (CHF, pneumonia,
cancer tumors, Pulmonary Embolism)
- Patho: Transdative ( non inflammtory causes) e.g
CHF and decreases in oncotic pressure.
EXUDATIVE ( caused by inflammatory probs)
- S/S: pleuratic pain on inspiration, asysmetric chet
expansion, dyspnea, SOB cause of the
accumulation of fluid, absent breath sounds,
RESP ACIDOSIS.
- Intervention: thoracentesis, chest tube drainage,
cough and breathing exercise, splinting chest
 MED SURGE II: RESP
SYSTEM
PNEUMOTHORAX: ( most common reason for inserting
CT)
- WHAT IS IT ? : accumulation of air in the pleural space,
increasing the pressure (atm pressure disrupt the
negative pressure in the lungs causing collapse). The
excess air in the pleural space limits lung expansion
causing collapse.
- PATHO: trauma ( open chest wound), thoracentesis,
infection, trauma. Air enters on inspiration bt cannot
escape during expiration
- S/S: shift of the mediastinum, trachea, larynx to the
unaffected side, tachypnea, tachycardia, dyspnea,
hypoxia, asymmetrical chest wall expansion, drop in
CO, hypoxia.
- INTERVENTION: tell doc, oxy therapy, TCDB
 MED SURGE II: RESP
SYSTEM
HEMOTHORAX: accumulation of blood in the pleural
space
- S/S: absent breath sounds even when chest tube is
insterted. * HYPOVOLEMIA FROM THE BLOOD LOSS.

PLEURISY:
- Edema and congestion of the pleura. Pleura is inflamed
and stretched. ** KEY SYMPTOM= PAIN stabbing
sensation made worse by beathing. Confirmation of Dx
by chest X-Ray

 EMPYEMA: accumulation of purulent fluid in the

pleural cavity. Complication of * bacterial pneumonia
COPD:
- WHAT IS IT ?? : group of diseases that cause obstruction of
airway ( CHRONIC BRONCHITIS, EMPHYSEMA). * hypoxia is
the drive to breathe ( due to the prolonged high CO2 levels).
- Patho: * smoking *inhaled irritants ( occupational exposure).
- S/S: wheezing, chronic cough (hemoptysis), prolonged
expiration time, *barrel chest: over inflation of the chest and
distended neck veins (key physical sign) , clubbing of
fingers, accessory muscles to breathe, * rhonchi
- INTERVENTIONS: * give oxygen at low levels so that you
don’t decrease hypoxic drive. * pursed lip breathing, high
fowlers position, fluids to liquefy mucus, postural drainage
45mins before meals, humidified oxygen, steroids,
bronchodilators, beta agonist, anticholinergics
 COPD MEDS
BRONCHODILATOR:
- Reduces the smooth muscle tone,
improving breathlessness.
ANTICHOLINERGICS:
- Prevent bronchi constriction by
inhibiting acetylcholine, they may also
reduce excess mucus production. *
have no effect on pulmonary vessels so
have no effect on oxygen levels.
THEOPHYLLINE: range 10-20
- Sympathomimetic bronchodilators.
- * watch for toxicity: s/s= vomitting,
hyperactivity and tachycardia
EMPHYSEMA:

WHAT IS IT ?: prob with the alveoli, they lose elasticity,

become over distended to allow more air into the lungs
and eventually alveoli destruction. Types: *Panlobular=
entire alveolar destruction, Paraseptal= restricted to
alveolar ducts and sacs.
S/S: air hunger, use of accessory muscles to breathe,
patient usually sit in a position leaning forward. Air
trapping CO2 levels >45mmHg.
 CHRONIC BRONCHITIS:
- WHAT IS IT ?: inflammation of the bronchiole and
bronchi. * no effect on the alveoli. excess mucus
production, impaired ciliary function, and decrease in
mucus production.
- S/S: excessive sputum production, cyanosis, cough,
excessive intolerance, wheezing, SOB, dependent
edema. * crackles, * resp acidosis.
- treatment: steroids, bronchodilators, mucomyst,
antibiotics,
 MED SURGE II: RESP SYSTEM

ASTHMA:
- WHAT IS IT ??:CHRONIC INFLAMMATION OF THE AIRWAY.
narrowing of the airway, caused by constriction of
smooth muscle of the bronchioles and bronchi,
excessive mucus production, edema of the resp tract.
- S/S: wheezing, chest tightness, SOB, cough
EXTRINSIC: aggrevated by inflammatory response to
allergens
INTRINSIC: chemicals ( infection, air pollution, exercise,
stress) interact with the ANS and cause reacton.
INTERVENTION: beta 2 adrenergic agonist, antibiotics,
bronchodilators, expectorants, inhaled steroids to
prevent edema. Oxygen
- DIAGNOSTIC TESTS: ABG’s, resp acidosis in chronic
asthma
 MED SURGE II: RESP SYSTEM

ATELECTASIS:
- What is it??? : incomplete expansion of the
alveoli or collapse of
- PATHO/ETIOLOGY: bronchiole obstruction of the
lungs due to the accumulations of secretions
( e.g post op), excess pressure on lung tissue
e.g with PLEURAL effusion.
- S/S: nasal flaring, hypoxia, asymetrical chest
wall expansion, hypoventilation
- INTERVENTION: incentive spirometrey, TCDB,
turn patient on the unaffected side to promote
drainage, hydration, encourage ambulations.
 MED SURGE II: RESP SYSTEM

ASTHMA:
STATUS ASTHMATICUS:
- NPO, IV FLUIDS FOR HYDRATION, IV
BRONCHODILATORS & STEROIDS.
- * INABILITY TO HEAR WHEEZING IN A
PATIENT WITH ASTHMA INDICATES RESP
OBSTRUCTION.
- * WATCH FOR SUPRASTERNAL
RETRACTION IN INHALATION.
- CAN CAUSE CARDIAC OR RESP ARREST.
- * RESP ALKALOSIS.
 PNEUMONIA
 ETIOLOGY: Viral in infants and young children
fungal in the immunocompromised
Bacterial: ( pneumonoccocus, klebsiella, strep,
staph aureus.
 S/S: older patients may present with confusion
at first. Primary symptoms, dyspnea, high WBC
and fever chest pain cough with sputum:-
SPTUM COLORS & CASUATIVE AGENT:
- STAPH : yellow
- PNEUMOCCOCAL: rusty, blood streaked
- Klebsiella: gel red
 INTERVENTIONS: TCDB, semi fowlers, increase
fluids * wash hands sepsis ( tachy, elevated
WBC, increase HR), * do not start antibiotics
before culture sensitivity testing has been done.
* drug resistance probs in the elderly.
 TB
PATHO: resp droplets, inhaled and make their
way to the bronchioles and alveoli. AGENT:
MYCOBACTERIUM TUBERCULOSIS.
S/S: low fever, night sweats, productive or non
productive cough. primary infection: may be
asymptomatic and infection lies dormant
Latent Infection: granulomas form, lesions
formed on primary infection are encased.
Post Primary: lesions rupture, active and
infectious stage. (+) smear = contagious.
Complications of TB: * cardiac tamponade,
renal and liver failure
DIAGNOSTICS: CXR, sputum culture,
Mantoux test ( not 100% reliable because if
immunocompromised it gives you a false
positive).
 TB

MEDICAL INTERVENTION: INH, Rifampin,

Pyrazinamine, Ethambutol if drug resistance
is suspected. *streptomycin disrupts the
protein synthesis. Therapy usually lasts
6months.
Nursing Interventions: cover mouth,
isolation ( after diagnosis has been
confirmed by positive sputum culture) in
negative pressure room , patients will stop
isolation is they have 3 (-) sputum cultures,
monitor liver panels.
 LUNG CANCER

PATHO: * smoking, occupational

exposure to irritants.
S/S: may be asymptomatic, and find out
in just a routine chest X-ray. Persistent
chronic cough, hemoptysis, recurrent
pneumonia and bronchitis, metastasis in
the liver, bone, brain and lymph nodes
usually.
MEDICAL INTERVENTION: surgery,
radiation, chemo
NURSING INTERVENTIONS: TCDB,
incentive spirometer, if post op position
in semi fowlers, encourage ambulation,
 CYSTIC FIBROSIS
PATHO: GENETIC, MALFUNCTION OF THE *EXOCRINE
GLAND. * AFFECTS MAINLY THE LUNGS, PANCREASE AND
SWEAT GLANDS.
DIAGNOTICS: sweat- chloride test ( normal = 5-35mEq/L)
S/S: * usually in whites, diagnosed in childhood, * thick
excess mucus production , causing atelectasis and
reoccurring resp tract infections. Malfunction of the
pancreas causes inadequate enzymes for digestion,
SWEAT GLANDS: excretion of excessive amounts of NaCl.
* barrel chest * foul smelling stool due to increased fat in
stool and undigested food. * taste like salt
MEDICAL TREATMENT: antibiotics, mucolytics, * control
infection in the lungs
NI: postural drainage, high calorie & protein meals, fat
soluble vitamins A,D,E,K. Percussion and Vibration
 PULMONARY EMBOLIM (PE)
WHAT IS IT??? Obstruction of the pulmonary artery . Usually
caused by a blood clot. * right lower lobe usually affected.
Some patients can die in 2hrs * usually caused by DVT.
ETIOLOGY: *DVT, surgery, prolonged periods of sitting
(VENOUS STASIS) e.g on a plane, pregnancy
,thromboembolism, obesity, HYPERCOAGGULATION
( dehydration, increased platelet count, contraceptives),
VASCULAR INJURY e.g IV catheters
(THE THREE MAJOR CAUSES ARE CALLED: VIRCHOWS TRIAD)
PATHO: thrombi changes to embolus, travels to the right
side of the heart and blocks the whole lung, part or just one
lobe no blood flow to exchange gases to that area dead
space. Alveoli stop producing surfactant causing collapse.
S/S: * sudden pleuratic chest pain, hypotension, syncope,
tachycardia, dyspnea,
 PULMONARY EMBOLIM (PE)

INTERVENTION:
- Oxygen
- Anticoaggulants ( Warfarin to prevent more
clots)
- Heparin – PTT ( antidote *protamine sulfate)
prevents the conversation of prothrombin
into thrombin
- Coumadin- PT/INR ( antidote * vitamin K) 2.0-
3.5 prevents the formation of new clots.
Interfers with clotting by inhibiting the
activity of Vitamin K.
- THROMBOLYTIC ENZYMES: * STREPTOKINASE
( dissolves existing thrombi).
 MED SURGE II: RESP
DYSPNEA:
SYSTEM
- measured by level of daily activity @ the point
when the patient feels the SOB.
BREATH SOUNDS:
- CRACKLES: = air passing through fluid, heard on
the lung bases, heard on INSPIRATION.
- RHONCHI ( SONOROUS): heard on expiration, air
passing through fluid in the upper airway; sounds
like snoring.
- SIBILIANT ( WHEEZING) = airway obstruction,
musical sound.
- PLEURAL FRICTION RUB= inflammation of the
pluera. Harsh rubbing sound heard with both ins
& expiration.
 MED SURGE II: RESP
SYSTEM
CHEST PAIN:
- Associated w? : fever, chills, cough, pleuratic
( sharp stabbing pain).
HEMOPTYSIS: blood in sputum. Assess
whether it is coming from the lungs or the
nose. Blood from lungs = bright red; OLD
BLOOD= dark brown.
CENTRAL CYANOSIS = discoloration of the
mouth and lips and the buccal mucosa
PERIPHERAL CYANOSIS= earlobes,
extremities and nail beds (clubbing, spongy
spoon like fingernails. Angel > 180 degrees)
 MED SURGE II: RESP
SYSTEM
 MEASUREMENTS OF PULMONARY FUNCTION:
- TOTAL LUNG CAP= volume of air in the lungs after
max inspiration
- VITAL CAPACITY= max volume of air exhaled
from the point of max inspiration.

 HYPERCAPNIA = inability of the body to sustain

the adequate levels for ventilation due to one or
three centres in charge of respiration ( CNS-
pons/medulla; PNS- chest bellows; airway
component. Measured by ABG’s).
 MED SURGE II: RESP
HYPOXIA:
SYSTEM
- Decrease in tissue oxygenation
- HYPOXEMIA= low levels of Oxygen in the blood.

Oxygen therapy interventions: oxygen supplement,

tracheostomy, chest tube
Give oxygen at a rate greater than 21% if hypoxia. * do
not give COPD patient more than 2L oxygen, because it
depresses their resp drive.
 COMPLICATION OF OXYGEN THERAPY = TOXICITY
OXYGEN TOXICITY = damage to lung tissue if exposed
to high levels of oxygen, atelectasis, alveolar collapse,
resp difficulty and fatigue, * SUB STERNAL PAIN.
 INSUFFICIENT OXYGEN
EARLY SIGNS
LATE SIGNS

• MENTALLY: confusion, • MENTALLY: seizures,

restlessness, HA lethargy, coma and
• BP: tachycardia brain swelling.
• PULSE: rising and • BP: bradycardia
bounding • PULSE: falling and
• RESP: rapid shallow
• SKIN: cool and • RESP: slowed
clammy • SKIN: cyanosis
 TRACHEOSTOMY &
SUCTIONING
TRACHEOSTOMY: artifial airway created in
the trachea.
- Finistrated tracheostomy allows the patient
to talk.
- INTERVENTIONS: watch for infection, use
humidifier when delivering oxygen, monitor
for cyanosis, keep well hydrated.
SUCTIONING:
- Purpose: clear airway
- Prevent hypoxia by monitoring pulse ox
during suctioning, suction for no more than
10-15seconds at a time, give oxygen
before and during suctioning.
 CHEST TUBE
FUNCTION: restores negative intrapleural pressure
(by removing air or fluid from the lung) in the
Lungs therefore causing lung expansion.
- INDICATION: pleural effusion, hemothorax,
pneumothorax, empyema, cardiothoracic surgery
( * open heart surgery to prevent cardiac
tamponade).
- * inserted between the 5th and 6th intercoastal
space, apply vaseline gauze, patient may feel a
pulling sensation when fluid is being drained.
 CHEST TUBE
INTERVENTIONS
 position patient with HEMOTHORAX= high fowlers.
 Position patient with pneumothorax= semi- high fowlers.
 Unit must be 1ft below patient to prevent backflow.
Assess for SUB CUTANEOUS EMPHYSEMA by palpating the
skin around the chest tube area ( will feel like rice crispies
under the skin).
 TEACH: splinting, cough and deep breathing, use
incentive spirometer 10times/hr
 If dislodged from patient= cover site with occlusive gauze
( vaseline gauze) and call doc
 If dislodged from unit= submerge 1 inch in sterile water or
sterile saline to create a liquid seal.
 Assess drainage and document q4hrs
Call doc if: drainage is >3ml/kg/hr for >2hrs or if fluid
turns from serous (white) to sanguineous ( bloody)